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      • KCI등재

        Nomenclature of ISCR1 Elements Capable of Mobilizing Antibiotic Resistance Genes Present in Complex Class 1 Integrons

        Seung Ghyu Sohn,Jae Jin Lee,Jae Seok Song,이정훈,Ha Ik Sun,Kwang Seung Park,Il Kwon Bae,이정현,정병철,이상희 한국미생물학회 2009 The journal of microbiology Vol.47 No.4

        The dissemination of many antibiotic resistance genes has arisen among members of the family Enterobacteriaceae. The dissemination mechanism of these antibiotic resistance genes is closely linked with insertion sequence common region 1 (ISCR1). Thus, caution must be taken in clinical settings to prevent further dissemination of these antibiotic resistance genes. A nomenclature system of ISCR1 variants, important for the antibiotic resistance dissemination, was proposed. The proposed system can designate all ISCR1 variants on the basis of the detection time and by considering amino-acid substitution(s) compared with ISCR1a. This nomenclature system of ISCR1 variants can be applied to 19 groups (ISCR1 to ISCR19) of the ISCR family and help some researchers to correctly designate new ISCR subgroups.

      • KCI등재

        Helicobacter pylori 감염의 치료와 Clarithromycin 내성간의 연관성

        손승규,이종화,이정훈,이상희,Sohn Seung Ghyu,Lee Jong Hwa,Lee Jung Hun,Lee Sang Hee 한국미생물학회 2005 미생물학회지 Vol.41 No.3

        본 연구를 수행하기 전에 H. pylori에 대한 어떠한 치료도 받지 않은 114명의 소화기 궤양 환자들을 내시경 검사를 하는 동안, 114개의 H. pylori 균주를 위 전정부로부터 분리하였다. H. pylori를 검출하기 위하여 rapid urease test, SSA와 cagA 유전자의 PCR증폭을 수행하였고, CagA 발현 검출을 위하여 Western blot을 수행하였다. H. pylori에 감염된 환자들은 omeprazole. clarithromycin (a macrolide), amoxicillin을 모두 사용하는데 3제 요법(triple therapy)으로 치료하였다. 치료가 중단되고 6주 후에 내시경 검사에서 세균 박멸률을 측정하였다. 내성률은 각각 clarithromycin이 $20.2\%$. amoxicillin이 $0.0\%$였다. Clarithromycin 내성은 H. pylori의 23S rRNA 유전자에 있는 A2142G돌연변이에 의한 것이 $87\%$이었다. A2142G돌연변이의 clarithromycin의 MIC값($32\~>256\;{\mu}g\ml$)은 A2143G돌연변이의 MIC값($4\~128\;{\mu}g/ml$)보다 더 높았다. Clarithromycin에 감수성을 가진 H. pylori는 박멸되었으나 clarithromycin내성을 가진 H. pylori는 박멸되지 않았다(P = 0.0001). 이러한 결과들은 CagA 발현에는 어떠한 영향도 받지 않았으며 H. pylori의 clarithromycin 내성은 치료 실패의 가장 중요한 이유임을 제시하였다. 우선적으로 실시되는 생검 배양에 대한 H. pylori의 항생제 감수성 시험은 감염된 환자들에 대한 3제 요법을 선택하기 이전에 필히 실시되어야 하며 국내에서 clarithromycin에 대한 1차 내성의 높은 빈도는 H. pylori의 감염증 치료에 심각한 문제점을 야기시켰다. H. pylori strains were isolated from antral biopsies taken during upper endoscopy in 114 dyspeptic patients with no previous therapy against H. pylori. Rapid urease test, PCR amplification of SSA and cagA gene for H. pylori detection, and Western blot for CagA expression detection were performed. H. pylori infected patients were treated with omeprazole, clarithromycin (a macrolide), and amoxicillin. At 6 weeks after the discontinuation of therapy, the bacterial eradication rate was determined by endoscopy. The resistance rate to clarithromycin and amoxicillin was $20.2\%$ and $0.0\%$, respectively. The clarithromycin resistance was mainly caused by the A2142G mutation in the 23S rRNA gene of H. pylori. MICs of clarithromycin for the A2142G mutant isolates were significantly higher than MICs for the A2143G mutant isolates. H. pylori eradication was obtained in all patients with clarithromycin-susceptible isolates but not in patients with clarithromycin-resistant isolates (P = 0.0001). These results did not appear to be biased by any differences in CagA expression. The resistance of H. pylori to clarithromycin included in the therapeutic regimens is the most important reason for treatment failure. H. pylori antimicrobial susceptibility testing of the gastric biopsy culture should be performed before choosing the first triple therapy in infected patients and the increase in prevalence of clarithromycin resistance in Korea was problematic.

      • SCIESCOPUSKCI등재
      • SCIESCOPUSKCI등재

        Outbreaks of Imipenem-Resistant Acinetobacter baumannii Producing Carbapenemases in Korea

        Jeong Seok-Hoon,Bae Il-Kwon,Park Kwang-Ok,An Young-Jun,Sohn Seung-Ghyu,Jang Seon-Ju,Sung Kwang-Hoon,Yang Ki-Suk,Lee Kyung-Won,Young Dong-Eun,Lee Sang-Hee The Microbiological Society of Korea 2006 The journal of microbiology Vol.44 No.4

        Among 53 Acinetobacter baumannii isolates collected in 2004, nine imipenem-resistant isolates were obtained from clinical specimens taken from patients hospitalized in Busan, Korea. Nine carbapenemase-producing isolates were further investigated in order to determine the mechanisms underlying resistance. These isolates were then analyzed via antibiotic susceptibility testing, microbiological tests of carbapenemase activity, pI determination, transconjugation test, enterobacterial repetitive consensus (ERIC)-PCR, and DNA sequencing. One outbreak involved seven cases of infection by A. baumannii producing OXA-23 ${\beta}-lactamase$, and was found to have been caused by a single ERIC-PCR clone. During the study period, the other outbreak involved two cases of infection by A. baumannii producing IMP-1 ${\beta}-lactamase$. The two clones, one from each of the outbreaks, were characterized via a modified cloverleaf synergy test and an EDTA-disk synergy test. The isoelectric focusing of the crude bacterial extracts detected nitrocefin-positive bands with pI values of 6.65 (OXA-23) and 9.0 (IMP-1). The PCR amplification and characterization of the amplicons via direct sequencing showed that the clonal isolates harbored $bla_{IMP-1}$ or $bla_{oxA-23}$ determinants. The two clones were characterized by a multidrug resistance phenotype that remained unaltered throughout the outbreak. This resistance encompassed penicillins, extended-spectrum cephalosporins, carbapenems, monobactams, and aminoglycosides. These results appear to show that the imipenem resistance observed among nine Korean A. baumannii isolates could be attributed to the spread of an IMP-lor OXA-23-producing clone. Our microbiological test of carbapenemase activity is a simple method for the screening of clinical isolates producing class D carbapenemase and/or class B $metallo-{\beta}-lactamase$, in order both to determine their clinical impact and to prevent further spread.

      • KCI등재

        Outbreaks of Imipenem-Resistant Acinetobacter baumannii Producing Carbapenemases in Korea

        정석훈,배일권,Kwang Ok Park,Young Jun An,Seung Ghyu Sohn,Seon Ju Jang,Ki Suk Yang,용동은,성광훈,이경원,이상희 한국미생물학회 2006 The journal of microbiology Vol.44 No.4

        Among 53 Acinetobacter baumannii isolates collected in 2004, nine imipenem-resistant isolates were obtained from clinical specimens taken from patients hospitalized in Busan, Korea. Nine carbapenemase-producing isolates were further investigated in order to determine the mechanisms underlying resistance. These isolates were then analyzed via antibiotic susceptibility testing, microbiological tests of carbapenemase activity, pI determination, transconjugation test, enterobacterial repetitive consensus (ERIC)-PCR, and DNA sequencing. One outbreak involved seven cases of infection by A. baumannii producing OXA-23 β-lactamase, and was found to have been caused by a single ERIC-PCR clone. During the study period, the other outbreak involved two cases of infection by A. baumannii producing IMP-1 β-lactamase. The two clones, one from each of the outbreaks, were characterized via a modified cloverleaf synergy test and an EDTA-disk synergy test. The isoelectric focusing of the crude bacterial extracts detected nitrocefin-positive bands with pI values of 6.65 (OXA-23) and 9.0 (IMP-1). The PCR amplification and characterization of the amplicons via direct sequencing showed that the clonal isolates harbored blaIMP-1 or blaOXA-23 determinants. The two clones were characterized by a multidrug resistance phenotype that remained unaltered throughout the outbreak. This resistance encompassed penicillins, extended spectrum cephalosporins, carbapenems, monobactams, and aminoglycosides. These results appear to show that the imipenem resistance observed among nine Korean A. baumannii isolates could be attributed to the spread of an IMP-1- or OXA-23-producing clone. Our microbiological test of carbapenemase activity is a simple method for the screening of clinical isolates producing class D carbapenemase and/or class B metallo-β-lactamase, in order both to determine their clinical impact and to prevent further spread.

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